The highlights of our study on the molecular mechanism of tumor reversion using mouse neuroblastoma cell system as a model can be summarized as follows: 1. We have shown that the differentiation of mouse neuroblastoma is accompanied by significant alterations of polayamine metabolism which include (a)\a decrease of cellular ornithine decarboxylase (ODC) activity, (b)\a five-fold decrease in spermidine content, (c)\a decrease in putrescine uptake, (d)\a decrease in the asparagine-dependent ODC induction, (e)\a decrease in the metabolic labeling of the 18,000 dalton protein by [14C] putrescine and (f)\an increse of the conversion of putrescine to amino acids via alpha-aminobutyric acid. 2. The essential role of polyamines and ODC in the differentiation of mouse neuroblastoma cells is further suggested by the findings that alpha-fluoromethylornithine (alpha-FMO), a suicidal enzyme inhibitor of ODC, plus suboptimal concentration of dibutyryl cAMP (0.1 approximately 0.2 mM) can cause maximal differentiation of neuroblastoma cells and the differentiation can be blocked by exogenously adding putrescine or spermidine. A potential use of alpha-FMO in the combination chemotherapy of neuroblastoma and related tumor diseases may be explored. 3. We have completed the surface proteins cataloging work for both undifferentiated and differentiated mouse neuroblastoma cells. 4. We have identified the regulatory subunit of Type 1 cAMP-dependent protein kinase as the specific protein which increases two to threefold during the differentiation of mouse neuroblastoma cells. Currently, we focus our effort on the molecular properties and functions of the 18,000 dalton protein which is specifically and metabolically labeled by polyamines.